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乳腺浸润性导管癌组织中ALDH1+/CD133+干细胞样细胞与血管生成的关系[J]. 肿瘤防治研究, 2015, 42(07): 706-711. DOI: 10.3971/j.issn.1000-8578.2015.07.014
引用本文: 乳腺浸润性导管癌组织中ALDH1+/CD133+干细胞样细胞与血管生成的关系[J]. 肿瘤防治研究, 2015, 42(07): 706-711. DOI: 10.3971/j.issn.1000-8578.2015.07.014
Relationship of ALDH1+/CD133+ Stem Cell-like Cells with Angiogenesis in Breast Invasive Ductal Carcinoma Tissues[J]. Cancer Research on Prevention and Treatment, 2015, 42(07): 706-711. DOI: 10.3971/j.issn.1000-8578.2015.07.014
Citation: Relationship of ALDH1+/CD133+ Stem Cell-like Cells with Angiogenesis in Breast Invasive Ductal Carcinoma Tissues[J]. Cancer Research on Prevention and Treatment, 2015, 42(07): 706-711. DOI: 10.3971/j.issn.1000-8578.2015.07.014

乳腺浸润性导管癌组织中ALDH1+/CD133+干细胞样细胞与血管生成的关系

Relationship of ALDH1+/CD133+ Stem Cell-like Cells with Angiogenesis in Breast Invasive Ductal Carcinoma Tissues

  • 摘要: 目的 探讨乳腺浸润性导管癌组织中肿瘤干细胞标志物ALDH1、CD133的表达及其与肿瘤血管生成的关系。方法 应用免疫组织化学双染法检测120例乳腺浸润性导管癌组织中ALDH1+/CD133+ 干细胞样细胞,单染法检测血管性标记CD34、CD105及VEGF的表达情况。统计ALPH1+/CD133+干细胞样细胞与临床病理因素;CD34、CD105与VEGF的关系。结果 25.83%(31/120)的病例存在ALDH1+/CD133+干细胞样细胞,ALDH1+/CD133+干细胞样细胞与ER、VEGF的表达及MVD均相关(P<0.05),但与年龄、肿瘤直径、PR、Her-2、组织学分级及淋巴结转移均无关(P>0.05)。结论 乳腺浸润性导管癌组织中ALDH1+/CD133+干细胞样细胞可能通过调节VEGF的表达促进肿瘤新生血管的生成。

     

    Abstract: Objective To explore the expression of cancer stem cell markers, ALDH1 and CD133, in breast invasive ductal carcinoma tissues and elucidate their relationship with angiogenesis. Methods The expression levels of ALDH1/CD133, CD34, CD105, and VEGF were detected by immunohistochemical double and single staining methods in 120 specimens of breast invasive ductal carcinoma. Results The expression rate of ALDH1+/CD133+ cells in the cancer tissues was 25.83%(31/120). It was closely associated with microvessel density(MVD), VEGF and ER expression (P<0.05), while no significant association with age, tumor size, PR, Her-2, histological grade or lymph node metastasis(P>0.05). Conclusion In breast invasive ductal carcinoma tissues, ALDH1+/CD133+ stem cells-like cells may promote angiogenesis by improving the expression of VEGF.

     

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